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Related Concept Videos

Alzheimer's Disease: Overview01:26

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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The amygdala is a small, almond-shaped structure responsible for processing and storing memories, particularly those linked to emotions like fear and stress. It plays an essential role in the brain's response to emotionally significant events and often enhances memory formation by triggering stress hormone release. The amygdala is vital for encoding and retrieving memories associated with fear or stress, a process that is adaptive by helping organisms avoid dangerous situations.
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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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AGEs RAGE Pathways: Alzheimer's Disease.

Shubhrat Maheshwari1

  • 1Faculty of Pharmaceutical Sciences, Rama University, Kanpur, Uttar Pradesh, India.

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Summary
This summary is machine-generated.

Alzheimer disease (AD) involves amyloid plaques and neurofibrillary tangles. This review focuses on advanced glycation end products (AGEs) and RAGE pathways contributing to AD pathogenesis.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer disease (AD) is characterized by neurofibrillary tangles and amyloid plaques, primarily driven by beta-amyloid peptide (Aβ) deposition.
  • Aβ production involves amyloid precursor protein (APP) modification and protein misfolding, with presenilin 1 (PS1) and beta-site APP-cleaving enzyme (BACE) as key secretases.
  • Oxidative stress, reactive oxygen species (ROS), and advanced glycation end products (AGEs) exacerbate neurotoxicity in AD.

Approach:

  • This review compiles recent research on the roles of AGEs and their receptor, RAGE, in AD pathogenesis.
  • It examines the interplay between AGEs, Aβ, and neurotoxicity.
  • The focus is on understanding the AGEs/RAGE pathway's contribution to AD.

Key Points:

  • Amyloid fibrils, though composed of self-proteins, are poorly cleared by the immune system.
  • PS1 and BACE activity significantly increases Aβ production.
  • AGEs and Aβ synergistically enhance neurotoxicity.

Conclusions:

  • The AGEs/RAGE pathway represents a significant area of investigation for understanding and potentially targeting AD.
  • Further research into AGEs and RAGE is crucial for developing novel therapeutic strategies for Alzheimer disease.